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MCB 2000 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

F0 Domain

A
  • imbedded in the intermembrane
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2
Q

Gamma Subunit

A
  • In the F1 domain of ATP synthase
  • Connected to the C-ring and to the alpha-subunit and beta-subunit of the F1 domain (matrix side)
  • Is the driving force of the C-ring rotation
  • Influences the conformation of the beta-subunit
  • Propelled by the movement of protons
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3
Q

Alpha Subunit

A
  • Acts as spacers between the beta-subunits
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4
Q

Beta Subunit

A
  • Can exist in three different conformations
    • Open (O) - going to release the ATP and be open for ADP + Pi to enter
    • Loose (L) - going to bind ADP + Pi
    • Tight (T) - converts ADP + Pi to ATP
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5
Q

Respiratory Control

A
  • ADP concentration controls rate of O2 consumption
  • ATP and ETC are coupled
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6
Q

Glycerol-3-Phosphate Shuttle

A
  • Predominant in the muscle
  • Shuttles FAD and FADH2
  • Will yield less ATP than Malate-Aspartate Shuttle because of the use of FAD
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7
Q

Malate-Aspartate Shuttle

A
  • Predominant in the liver (and heart)
  • Uses NADH to accept cytoplasmic electrons
  • Conserves NADH and no ATP is lost
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8
Q

ATP Synthesis Inhibitors

A
  • Inhibition of the ETC at any point (respiratory inhibitors)
    • Anything that prevents O2 from accepting e-s
  • Direct inhibition of ATP synthase
    • This means you are going to have a buildup of ADP, but the ETC will back up as well since the e- carriers are not being re-oxidized
    • If you don’t make ATP, then the ETC is not going to keep going, there is a limit for the pmf to be reached
  • Disruption of proton gradient against IMM - uncouplers
    • ETC keeps going, but protons are coming back into the matrix but not by ATP synthase
    • pmf will decrease, driving the ETC, but no ATP will be made
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9
Q

Respiratory Inhibitors

A
  • Rotenone (pesticide), Amytal (barbituate)
    • Block at Complex I
    • The e- from NADH will not reach CoQ and therefore NADH will build up and negatively modify ETC
  • Antimycin (anti-fungal)
    • Block at Complex III
    • CoQ cannot deliver to Complex III and previous carriers will build up
  • Cyanide, Azide, CO
    • Target Complex IV
    • Cyanide and Azide keep iron in the oxidized, Fe3+ form
    • CO binds to Fe2+ so there is no back and forth redox reaction to be able to deliver those e- to O2
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10
Q

ATP Synthase Inhibitors

A
  • Oligomycin
    • Will attack F0 domain
  • DCCD
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11
Q

Uncouplers

A
  • Separate the tight coupling between ETC and oxidative phosphorylation (ATP synthesis)
  • Can be chemical or physiological
    • Chemical has no regulation, physiological does
  • Will keep consuming O2 and ETC will still run, to maintain pmf/proton gradient, but no ATP will be produced
  • Have an aromatic ring that allows it to interact with the inner membrane (different method of transportation for the protons across the membrane)
  • Physiological uncoupler: UCP-1
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12
Q

Glycogen

A
  • Polymer of glucose
  • Primarily stored in the liver and the skeletal muscle
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13
Q

Polysaccharides

A
  • All are made up of glucose
  • Cellulose - beta-1,4 linkage; primarily for structural support
  • Starch - primarily for energy storage
  • Glycogen - alpha-1,4 and alpha-1,6 linkage; branched
  • Amylopectin - alpha-1,4 and alpha-1,6 linkage; branched
  • Amylose - linear structure
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14
Q

Glycogen Synthase

A
  • major enzyme, that is going to catalyze the alpha-1,4 linkage
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15
Q

Glycogenin

A
  • Makes primer for glycogen synthesis
  • Can synthesize the primer de novo, but do not necessarily degrade the primer, so not always needed
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16
Q

Fatty Acid Synthesis

A
  • Major site is in the liver, not the adipose tissue
  • If insulin is present, then acetyl CoA will go into fatty acid synthesis
  • Acetyl CoA is the starting substrate
  • Occurs in the cytoplasm
  • NADPH is needed, not NADH because glyocolysis and fatty acid synthesis need to be able to take place at the same time and both happen in the cytoplasm
17
Q

Protein Phosphatase 1 (PP1)

A
  • Activated by the fed state, high I/G ratio
  • Dephosphorylates inactive gylcogen synthase and glycogen phosphorylase
18
Q

Glycogen Synthase Kinase

A
  • Deactivated in the fed state, high I/G ratio, but a protein kinase
  • Deactivation of glycogen synthase kinase allows glycogen synthase to remain dephosphorylated and active
19
Q

Inactive Glycogen Synthase

A
  • Dephosphorylated by PP1
  • Dephosphorylation of inactive glycogen synthase makes it become active
20
Q

Glycogen Phosphorylase

A
  • Dephosphorylated by PP1
  • Becomes inactive, so the new glycogen produced is not degraded
21
Q

NADPH

A
  • Reducing equivalent needed for fatty acid synthesis
  • Generated from two sources:
    • Malic enzyme, that converts malate into pyruvate
    • Pentose-P Pathway
22
Q

Acetyl CoA Carboxylase (ACC)

A
  • Adds a CO2 to acetyl CoA to produce malonyl CoA
  • Biotin is required as a co-enzyme for the production of malonyl CoA
  • Activation and rate limiting step in fatty aid synthesis
23
Q

Regulation of Acetyl CoA Carboxylase (ACC)

A
  • AMPK (AMP dependent protein kinase )- activated by AMP and is going to be inhibited by ATP; more active in the fasted state
  • Protein Phosphatase 2A (PP2A)
    • Stimulated by insulin
  • Citrate
    • Allosterically modified
    • Can bind to the phosphorylated, less active form of the enzyme, so it can activate the enzyme, but not 100%
      • Allows fatty acid synthesis to get started before dephosphorylating cascade finishes
  • Palmotyl CoA
    • Final product of fatty acid synthesis, and will allosterically modify ACC
24
Q

Glycerol Kinase

A
  • Only found in the liver, not adipose tissue
  • Glycerol can be recycled from the break down of triglycerides
  • Glycerol concentration does not strictly rely on glycolysis
25
Q

Phosphatidate

A
  • Common intermediate for phospholipids and triglycerides
  • Has its phosphate removed to produce DAG and a third fatty acid is added to create triaglycerol
26
Q

Chylomicron

A
  • Made in the small intestine
  • Transports dietary triglycerides
  • Become remnants when triglycerides are unloaded
27
Q

Very Low Density Lipid (VLDL)

A
  • Made in the liver
  • Transports newly synthesized triglycerides
  • Becomes IDL and eventually LDL after triglycerides are unloaded

MCB 2000 (4 decks)

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